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Other Data Relevant to an Evaluation of Carcinogenicity and Its Mechanisms

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Other Data Relevant to an Evaluation of Carcinogenicity and Its Mechanisms WOOD DUST 173 3.5 Experimental data on wood shavings It has been suggested in several studies that cedar wood shavings, used as bedding for animaIs, are implicated in the prominent differences in the incidences of spontaneous liver and mammar tumours in mice, mainly of the C3H strain, maintained in different laboratories (Sabine et al., 1973; Sabine, 1975). Others (Heston, 1975) have attributed these variations in incidence to different conditions of animal maintenance, such as food consumption, infestation with ectoparasites and general condition of health, rather than to use of cedar shavings as bedding. Additional attempts to demonstrate carcinogenic properties of cedar shavings used as bedding materIal for mice of the C3H (Vlahakis, 1977) and SWJ/Jac (Jacobs & Dieter, 1978) strains were not successful. ln no ne of these studies were there control groups not exposed to cedar shavings. 4. Other Data Relevant to an Evaluation of Carcinogenicity and its Mechanisms 4.1 Deposition and clearance 4.1.1 Humans No studies of the deposition of wood dust in human airways were available to the Working Group. Particle deposition in the airways has been the object of several studies (for reviews, see Brain & Valberg, 1979; Warheit, 1989). Large particles (? 10 ¡.m) are almost entirely deposited in the nose; the deposition of smaUer particles depends on size but also on flow rates and type of breathing (mouth or nose); there is also inter-individual variation (Technical Committee of the Inhalation Specialty Section, Society of T oxicology, 1987). Particles deposited in the nasal airways are removed by mucociliary transport (for reviews, see Proctor, 1982; Warheit, 1989). 4.1.2 Experimental systems No data on the deposition or clearance of wood dusts in animaIs were available to the W orking Group. 4.2 Toxic effects 4.2.1 Humans (a) Effects on the nase ln a cross-sectional study in eight furniture factories in Denmark, 68 workers were exposed to total dust at concentrations? 5 mg/m3 in 63% of the measurements (Solgaard & Andersen, 1975; Andersen et al., 1977). The workers were exposed to a variety of hardwoods, including teak, and to pine and composites, including chipboard and Masonite. Analysis of particle size ,,;ç:.:,...:,...._-- 174 lARC MONOGRAPHS VOLUME 62 showed that 33% of the particles were .; 5 !-m. These workers had significantly lower nasal mucociliary transport rates than a group not exposed to dust; there was also a concentration- dependent decrease in the rates of the exposed workers: mucostasis was found in 63% of workers exposed to an average of25.5 mg/m3 and in 11% ofthose exposed to 2.2 mg/m3 (mean concentration). Of ni ne subjects with mucostasis re-examined after 48 h with no exposure to wood, three still had mucostasis, while the six others had clearance rates within normal limits. Middle-ear inflammation and common co Ids were more frequently reported by people exposed to concentrations:; 5 mg/m3 than among those exposed to lower levels. The nasal mucociliary transport-rate was investigated in nine woodworkers, 48-66 years of age, with 6-27 years of employment in the furniture industry in England (Black et al., 1974). They had slower rates than 12 people not exposed to wood dust. Only the worker with the shortest length of employment (six years) had a clearance rate within normal limits. Three workers had complete stasis. The results of cytological examination of nasal smears were reported only for the exposed workers: squamous cells were found in four workers, cuboidal ceUs in one and 'less mature basal ceUs' in another. Boysen and Solberg (1982) studied 103 workers in five Norwegian furniture factories in a cross-sectional study. The subjects constituted about 60% of workers who had been emp10yed for at least 16 years. Ten retired workers and 54 people without nasal disease or an occupation associated with nasal cancer, who were not employed In woodworking industries, were examined. Nasal biopsy samples taken from the middle turbinate showed metaplastic squamous epithelium in 40% of the furniture workers and 17% of controls; the cOITesponding figures for dysplasia were 12 and 2%, respectively. Mechanical processing of wood was associated with histological changes of the nasal mucosa. Dysplasia occuITed in four of 15 furniture workers with exposure mainly to birch, spruce and pine and in nine of 84 exposed mai nI y to hardwoods. Nasal biopsy samples taken from the middle turbinate of 44 workers who had been exposed for 10-43 years to softwood dust but not to hardwood dust showed more changes than biopsy samples taken from age-matched men without nasal disease or an occupation associated with nasal cancer (mean score, 2.0 vers us 1.4; p 0: 0.05) (Boysen et al., 1986). Four woodworkers and no control had dysplasia; these four men had been exposed for 20 years (one man) and more than 26 years (three men). Nasal symptoms were more frequent among the furniture workers (14% versus 4%; p 0: 0.05). Biopsy samples were taken from the nasal mucosa of the middle turbinate, at least 5 mm behind the anterior curvature, of 45 randomly selected workers in five furniture factories and one parquet flooring factory and 17 hospital workers in Sweden (Wilhemsson & Lundh, 1984). The mean length of exposure was 15 years (range, 1-39 years). Metaplastic cuboidal epithelium was significantly more prevalent among the woodworkers (26/45 versus 4/17; p .; 0.05), and columnar epithelium was significantly less frequent (34/45 versus 17/17; p .; 0.05). The prevalence of metaplastic squamous epithelium was not significantly increased (9/45 versus 4/17), and that of goblet-cell hyperplasia was somewhat more frequent (10/45 versus 1/17). Cuboidal metaplasia of the nasal mucosa was found in 19 of 22 cases of ethmoidal adenocarcinoma associated with exposure to wood dust in Sweden (Wilhemsson et al.,1985c). Histological examination of non-tumour nasal mucosa from 22 woodworkers with ethmoidal WOOD OUST 175 adenocarcinoma, who had been exposed to wood dust for an average of 38 years (range, 18- 55 years), showed cuboidal metaplasia in 19; 16 also had dysplasia. A transitional zone with dysplastic cuboidal epithelium in continuity with the tumour was observed in 10 cases. Squamous metaplasia was also seen in five cases, but there were no cases of squamous dysplasia. A cross-sectional study in Germany involved 149 male workers with at least 15 years' exposure to wood dust in different industries and 33 workers with no exposure to dust or chemicals (contraIs); people who had worked as farmers, welders or metal workers or were exposed to cement dust were excluded. CUITent exposure to wood dust varied between ~ 1 mg/m3 and ? 5 mg/m3. Mucociliary clearance was not significantly different in workers exposed to unprocessed woods (oak, beech and softwood) and controls. Woodworkers with concomitant exposure to formaldehyde or chromium had decreased clearances (p = 0.04 and 0.01, respecti vely), and workers exposed to particle-board had slower mucociliary clearance. The findings in nasal biopsy samples taken from the middle turbinate were reported for various single ceU types (columnar-cell hyperplasia, squamous-ceU metaplasia, cuboid metaplasia) and mixed cell types (Wolf et al., 1994). (The Working Group noted the inadequate reporting of the histological classification and the high prevalence of squamous epithelial metaplasia in the control group. The Group analysed the data according to hyperplasia and metaplasia in single ceU types and found no significant differences between woodworkers and contraIs (Table 32). The odds ratios for woodworkers exposed to softwood or hardwood, but no additives, were 2.2 (95% CI, 0.81-6.2) for cuboid metaplasia, 0.40 (0.16-1.0) for squamous-cell metaplasia and 1.3 (0.47-3.5) for columnar-cell hyperplasia. Cuboid metaplasia was commoner in workers exposed to hardwood (3.5; 1.1-12), softwood (3.1; 0.77-12) or particle-board (25; 0.70-8.8) without additives than in controls but was significant only for workers exposed to hardwood.) ln a cross-sectional study of workers in furniture factories in Sweden who were exposed to formaldehyde alone and to formaldehyde plus wood dust, nasal discomfort was more frequent than in clerks (Holmström & Wilhemsson, 1988). The mean combined exposure to wood dust was 1.7 mg/m3 and that to formaldehyde was 0.25 mg/m3; however, the prevalence of symptoms was similar in workers exposed to formaldehyde alone (mean concentration, 0.26 mg/m\ Impaired mucociliar clearance in the nose was seen in 15% of the group exposed to wood dust plus formaldehyde, in 3% of controls and in 20% of those exposed to formaldehyde alone exposure (p ~ 0.05). Workers exposed to formaldehyde alone or to formaldehyde plus wood dust had significantly (p ~ 0.01) decreased sensitivity in an olfactory test in comparison with controls. Marked histological changes were seen in the nasal mucosa of 25% of people exposed only to formaldehyde (score, 2.2; p ~ 0.05), but the difference between those exposed to both formaldehyde and wood dust (64% (p ~ 0.01); score, 2.1) and the controls (53% (p ~ 0.01; score, 1.6) was not significant. No correlation was found between histological score and either duration or concentration of exposure (Holmström et al., 1989b). A total of 676 workers in 50 Swedish furniture factories were classified according to exposure to wood dust as 'heavily/moderately' or 'slightly/non-exposed' (Wilhemsson & Drettner, 1984) (the details of the classification were not reported). Nasal hypersecretion (20% ";.,..,~':",,,.',~ , _.~... Table 32. Frequency of histological findings in nasal biopsy sam -i pies from German woodworkers according to exposure 0' Type of Additives. No.b Histological finding wood Columnar- Squamous Cuboid Columnar Columnar Squamous Any Any Any cuboid Normal Dysplasia cel! metaplasia metaplasia hyperplasia, hyperplasia, metaplasia, columnar squamous metaplasia hyperplasia (2) (3) squamous cuboid cuboid hyperplasia metaplasia (3+5+6)" (1) (4) (5) (6) (1+4+5)" (2+4+6)" Hardwood No 31 6 1 5 3 1 6 10 10 12 9 3 Softood No 17 2 1 4 2 1 1 8 4 6 6 0 Paric1e- No 26 5 5 4 4 3 1 13 10 8 4 0 board -- Softood Yes 19 3 9 3 2 1 0 6 II 4 ~ Hardwood Yes 21 7 ;; 4 2 2 1 1 10 7 4 4 1 \.
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